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this. Immediately the waveform changed and the level of inhalational agents and EtCO2 went down. These changes were reproducible by changing the new sample line with the damaged one.

Subglottic stenosis and acute airway obstruction

Patient repositioning during general anesthesia is known to potentially cause injury. Repositioning of workstation may also jeopardize patient safety, as illustrated by this case. This case also emphasizes the significance of monitoring and alarm system during equipment movement under anesthesia. Alarms are often caused by manipulations performed by the medical staff working with the anesthesia workstation and may be annotated as “not relevant,”changing the significance of the alarm.[4] Also, awareness of this possible cause may help the clinician in narrowing down the reason of sudden decrease in EtCO2value due to such a mishap.

Sir, A 22-year-old female patient presented to the Emergency Department (ED) with acute breathlessness, stridor, agitation and altered sensorium. On applying pulse oximeter, her oxygen saturation (SpO2) was 74% on room air, which only marginally improved with supplemental O2. On auscultation, there were bilateral rhonchi. Patient’s medical records revealed subglottic laryngeal stenosis. A definitive tracheostomy was planned after securing airway with an emergency endotracheal intubation. A difficult airway cart was readied and an ear, nose & throat (ENT) surgeon was called to be standby for an emergency tracheostomy during endotracheal intubation in ED. Direct laryngoscopy revealed a modified Cormack and Lehane grade 3. A 4mm un-cuffed endotracheal (ETT) portex tube was successfully negotiated through the vocal cords, beyond the obstruction after repeated unsuccessful attempts to intubate with 5 and 4.5 millimeter (mm) ETT. At that moment, the loose ETT connector suddenly got disconnected from the tube. At the same moment, patient took a deep inspiratory breath, dragging the ETT along. On direct laryngoscopy, a miniscule rim of the proximal part of the disconnected ETT was visible just below the glottic opening. After oropharyngeal suctioning, adjusting head and neck position and proper external laryngeal manipulation, the tube was successfully retrieved using a pediatric magill’s forceps.

Extreme precaution during movement of the work station is needed to avoid such occurrences as a sudden decrease in EtCO2 value can lead to confusion especially during procedures like neurosurgery or where carbondioxide is used as insufflation gas. Prakash K. Dubey Department of Anesthesiology & Critical Care Medicine, Indira Gandhi Institute of Medical Sciences, Patna, Bihar, India Address for correspondence: Prof. Prakash K Dubey, E¾, Indira Gandhi Institute of Medical Sciences Campus, Sheikhpura, Patna - 800 014, Bihar, India. E-mail: [email protected]

References 1.




Nichols KP, Benumof JL. Biphasic carbon dioxide excretion waveform from a patient with severe kyphoscoliosis. Anesthesiology1989;71:986-7. Dorsch JA, Dorsch SE. Gas monitoring. Understanding Anesthesia Equipment. 5th ed. Philadelphia: Wolters Kluwer / Lippincott Williams & Wilkins; 2008. p. 685-727. Tripathi M, Pandey M. Atypical “tails-up” capnograph due to breach in the sampling tube of side-stream capnometer. J Clin Monit Comput 2000;16:17-20. Schmid F, Goepfert MS, Kuhnt D, Eichhorn V, Diedrichs S, Reichenspurner H, et al. The wolf is crying in the operating room: Patient monitor and anesthesia work station alarming patterns during cardiac surgery. Anesth Analg 2011;112:78-83.

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DOI: 10.4103/0970-9185.125735


Another 4 mm un-cuffed ETT was passed through the vocal cords, tube tightly secured and patient was ventilated with 100% oxygen. Her SpO2 picked up and became 100%. Subsequently definitive surgical tracheostomy was performed under local anesthesia and mild sedation with 8 mm cuffed tracheostomy tube to bypass the obstruction. Bilateral air entry was checked to be equal and adequate following administration of steroids and bronchodilators. Her sensorium was restored to normal with adequate spontaneous respirations. Her vital parameters were normal throughout (except for initial sinus tachycardia) and subsequently, her SpO2 became 100% on room air as well. She was later shifted to ward on T-piece after nebulization, tracheostomy suction and medical management. On detailed evaluation of her past histor y, she had pregnancy-induced hypertension and generalized edema during the last trimester of her pregnancy (3 months back). She developed postpartum jaundice and sepsis due to retained products of conception after normal vaginal delivery. She underwent management in the intensive care unit of a peripheral hospital for her condition for

Journal of Anaesthesiology Clinical Pharmacology | January-March 2014 | Vol 30 | Issue 1

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15 days, with intubation and ventilatory support, the records of which were not available. Two months later, she developed progressive hoarseness of voice and paroxysmal stridor, for which she consulted a local ENT surgeon. Video laryngoscopy findings performed then revealed: “Less movement of left Vocal cord on phonation. Normal morphology of lar ynx with narrowing of trachea just below the vocal cords, and was negotiable with a 5 mm bronchoscope only. Mucosa was inflamed and edematous. No growth was present. Rest of trachea, carina, bronchi and bronchioles were normal” [Figures 1 and 2].

in thickness, mildly compressing the trachea. On contrastenhanced CT of the neck, thickening of soft-tissue was noted in glottic and subglottic region, leading to narrowing of lumen. No obvious abnormal post-contrast enhancement was seen [Figures 3 and 4].

The patient was further investigated after been sent to the ward, with cervical X-rays (antero-posterior and lateral), indirect laryngoscopy (IDL) and computed tomography (CT) scan. On IDL, the glottic chink was inadequate and left vocal cord was immobile. On fiber-optic laryngoscopy, bilateral arytenoids were boggy and edematous. On X-ray neck, pre-vertebral soft-tissue shadow appeared increased

Patients with acquired stenosis are diagnosed from a few days to 10 years or more following the initial injury. The majority of cases are diagnosed within a year. Symptoms[1] include dyspnea (may be on exertion or with rest, depending on the severity of stenosis),stridor, hoarseness, brassy cough, recurrent pneumonitis, cyanosis. Management in all these situations needs to be prompt and definitive.[2] Since patient presented with acute airway obstruction possibly precipitated by a recent respiratory tract infection and consequent further narrowing,

Her post-tracheostomy course was uneventful in the ward, where her tracheostomy tube size was sequentially reduced and was finally decannulated. She was later discharged home after speech therapy and advised to follow-up regularly in ENT out-patient department.

Figure 1: Video laryngoscopy view taken by ear, nose and throat surgeon on first presentation of hoarseness postpartum Figure 2: Video laryngoscopy view as in Figure 1

Figure 3: Computed tomography scan of the neck taken during current evaluation of patient following tracheostomy

Figure 4: Computed tomography scan of the neck as in Figure 3

Journal of Anaesthesiology Clinical Pharmacology | January-March 2014 | Vol 30 | Issue 1


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Life-threatening severe sepsis following stapled hemorrhoidopexy

of rectal bleeding and associated prolapsing piles. He was receiving tablet metoprolol 50 mg and tablet amlodipine 5 mg since 2 years. On examination, he had 4th degree piles with a large external component. All pre-operative investigations were within the normal limit. Prophylactic antibiotics in the form of ceftriaxone and gentamycin were administered 30 min prior to surgery. A standard SH was performed under spinal anesthesia, but due to difficulty in closure some part of the hemorrhoids were also excised. During the intraoperative period, the patient felt uneasiness and some discomfort, hence was sedated with midazolam 1mg, but his mean arterial pressure (MAP) fell below 65 mm of Hg. He remained hypotensive for 10-12 min which was managed by administration of Ringer lactate 500 ml and tetrastarch 500 ml.This resulted in stabilisation of mean arterial pressure (MAP) above 70 mm Hg. A total amount of fluid administered during the intraoperative period was 1300 ml. Patient was shifted to the postoperative ward after completion of surgery. After 2 h of surgery, the patient complained of pain at the operative site. Intranasal butorphanol nasal spray 1 mg was administered to relieve the pain. Rest of the post-operative period on that day was uneventful. The patient did not pass urine until the morning of the next day. He also felt generalized weakness and breathlessness. At around 3 pm of the next post-operative day, his BP started falling to a MAP below 60 mm Hg despite administering 1L of 0.9% normal saline and hence he was shifted to intensive care unit within half an hour of developing hypotension. He did not pass urine until 4 pm inspite of being adequately hydrated and his BP at that time was 70 mm of Hg systolic. A central line was inserted and central venous pressure (CVP) guided fluid therapy started. We targeted a CVP of around 10 mm of Hg. Arterial blood gas (ABG) analysis was carried out and oxygen was administered through venturi mask at 6 L/min. Monitoring of non-invasive BP, pulse rate, heart rate, SpO2, temperature, continuous CVP, Urine output and abdominal girth was done. Patient’s vitals at that time were: Temperature-102°F, BP 74 mm of Hg (systolic), pulse rate 134 bpm, respiratory rate 32/min, SpO2 78% on 6 L/min O2 through mask, decreased air entry in both lung; fine crepts present, abdominal distension present, but no tenderness, and bowel sounds were absent. Urinary catheterization was performed. Electrocardiogram revealed sinus tachycardia; cardiac markers were sent and were within the normal limits

Sir, A 59-year-old hypertensive, non-diabetic male was admitted for stapled hemorrhoidopexy (SH) following a long history

At the same time, infusions of noradrenaline and dopamine were started. All routine investigations with coagulation profile and serum procalcitonin levels were also sent for early recognition of sepsis ABG report revealed metabolic

only a 4 mm ETT could be passed into the trachea,which relieved the obstruction momentarily. In our case, the problem was in the loose connection between the ETT and the standard connector. With patient taking a deep breath at the same time, there was a strong intrathoracic pressure pulling the un-cuffed ETT into the trachea. Postpartum patients who were on prolonged endotracheal intubation are more likely to develop subglottic stenosis.[3] A high index of suspicion is warranted with the onset of respiratory symptoms following a history of intubation, regardless of the duration of intubation. This case highlights the fact that subglottic stenosis can present as acute airway obstruction. Uma Hariharan Ex-Senior Resident, Department of Anesthesia and Intensive care Dr. Ram Manohar Lohia Hospital & Post Graduate Institute of Medical Education and Research, New Delhi, India Address for correspondence: Dr. Uma Hariharan, B H 41, East Shalimar Bagh, New Delhi - 110 088, India. E-mail: [email protected]

References 1. 2. 3.

Scholz A, Srinivas K, Stacey MR, Clyburn P. Subglottic stenosis in pregnancy. Br J Anaesth 2008;100:385-8. McCaffrey TV. Management of subglottic stenosis in the adult. Ann Otol Rhinol Laryngol 1991;100:90-4. Myer CM 3rd, O’Connor DM, Cotton RT. Proposed grading system for subglottic stenosis based on endotracheal tube sizes. Ann Otol Rhinol Laryngol 1994;103:319-23. Access this article online Quick Response Code:

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DOI: 10.4103/0970-9185.125736


Journal of Anaesthesiology Clinical Pharmacology | January-March 2014 | Vol 30 | Issue 1

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